Download BIOL260 Chapter 17 Lecture

ADAPTIVE IMMUNITY –
SPECIFIC DEFENSES OF THE
HOST
CHAPTER 17
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Q&A
 Why doesn’t the
adaptive immune
system normally
attack your own
body tissues?
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Immunity
 Innate immunity: Defenses against any pathogen
 Adaptive immunity: Induced resistance to a
specific pathogen
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Historical Development
 Pasteur observed immunity in chickens injected
with weakened pathogens
 Von Behring received the Nobel Prize for
development of antitoxin
 Ehrlich’s work led to the identification of antibodies
in serum
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Dual Nature of Adaptive Immunity
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Figure 17.8
Dual Nature of Adaptive Immunity
 T and B cells develop from stem cells in red bone
marrow
 Humoral immunity
 B cells mature in the bone marrow
 Chickens: Bursa of Fabricius
 Due to antibodies
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Dual Nature of Adaptive Immunity
 T and B cells develop from stem cells in red bone
marrow
 Cellular immunity
 Due to T cells
 T cells mature in the thymus
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The Nature of Antigens
 Antigen (Ag): A substance that causes the body to
produce specific antibodies or sensitized T cells
 Antibodies (Ab) interact with epitopes or antigenic
determinants
 Hapten: Antigen is combined with carrier
molecules
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Antigens
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Figure 17.1
Haptens
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Figure 17.2
The Nature of Antibodies
 Globular proteins called immunoglobulins
 The number of antigen-binding sites determines
valence
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Antibodies
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Figure 17.3a,b
Antibodies
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Figure 17.3c
IgG Antibodies
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Monomer
80% of serum Abs
Fix complement
In blood, lymph, and intestine
Cross placenta
Enhance phagocytosis; neutralize toxins and
viruses; protects fetus and newborn
 Half-life = 23 days
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IgM Antibodies





Pentamer
5–10% of serum Abs
Fix complement
In blood, in lymph, and on B cells
Agglutinates microbes; first Ab
produced in response to infection
 Half-life = 5 days
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IgA Antibodies


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Dimer
10–15% of serum Abs
In secretions
Mucosal protection
Half-life = 6 days
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IgD Antibodies





Monomer
0.2% of serum Abs
In blood, in lymph, and on B cells
On B cells, initiate immune response
Half-life = 3 days
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IgE Antibodies
 Monomer
 0.002% of serum Abs
 On mast cells, on basophils, and in
blood
 Allergic reactions; lysis of parasitic
worms
 Half-life = 2 days
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Activation of B Cells
 Major histocompatibility complex (MHC)
expressed on mammalian cells
 T-dependent antigens
 Ag presented with (self) MHC to TH cell
 TH cell produces cytokines that activate the B cell
 T-independent antigens
 Stimulate the B cell to make Abs
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Activation of B Cells
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Figure 17.6
Activation of B Cells
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Figure 17.4
Clonal Selection
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Figure 17.5
Activation of B Cells
 B cells differentiate into
 Antibody-producing plasma cells
 Memory cells
 Clonal deletion eliminates harmful B cells
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The Results of Ag-Ab Binding
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Figure 17.7
T Cells and Cellular Immunity
 T cells mature in the thymus
 Thymic selection eliminates many immature T cells
 T cells respond to Ag by T-cell receptors (TCRs)
 T cells require antigen-presenting cells (APCs)
 Pathogens entering the gastrointestinal or
respiratory tracts pass through
 M (microfold) cells over
 Peyer’s patches, which contain APCs
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M Cells on Peyer’s Patch
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Figure 17.9a
M Cells
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Figure 17.9b
T Helper Cells
 CD4+ or TH cells
 TCRs recognize Ags and MHC II on APC
 TLRs are a costimulatory signal on APC and TH
 TH cells produce cytokines and differentiate into
 TH1
 TH2
 Memory cells
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T Helper Cells
 TH1 produces IFN-gwhich activates cells related
to cell-mediated immunity, macrophages, and
Abs
 TH2 activate eosinophils and B cells to produce
IgE
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Activation of CD4+ T Helper Cells
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Figure 17.10
T Cytotoxic Cells
 CD8+ or TC cells
 Target cells are self carrying endogenous
antigens
 Activated into cytotoxic T lymphocytes (CTLs)
 CTLs recognize Ag + MHC I
 Induce apoptosis in target cell
 CTL releases perforin and granzymes
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T Cytotoxic Cells
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Figure 17.11
Apoptosis
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Figure 17.12
T Regulatory Cells
 Treg cells
 CD4 and CD25 on surface
 Suppress T cells against self
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Antigen-Presenting Cells
 Digest antigen
 Ag fragments on APC surface with MHC
 B cells
 Dendritic cells
 Activated macrophages
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A Dendritic Cell
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Figure 17.13
Activated Macrophages
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Figure 17.14
Natural Killer (NK) Cells
 Granular leukocytes destroy cells that don’t
express MHC I
 Kill virus-infected and tumor cells
 Attack parasites
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ADCC
 Antibody-dependent cell-mediated cytotoxicity
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Figure 17.15b
ADCC
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Figure 17.15a
Cytokines
 Chemical messengers
 Overproduction leads to cytokine storm
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Cells Communicate via Cytokines
Cytokine
Representative Activity
Interleukin-1 (IL-1)
Stimulates TH cells in presence of
antigens; attracts phagocytes
Interleukin-2 (IL-2)
Proliferation of antigen-stimulated
CD4+ T helper cells, proliferation
and differentiation of B cells;
activation of CD8+ T cells and NK
cells
Interleukin-12 (IL-12)
Inhibits humoral immunity;
activates TH1 cellular immunity
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Cells Communicate via Cytokines
Cytokine
Representative Activity
Chemokines
Induce the migration of leukocytes
TNF-α
Promotes inflammation
Hematopoietic
cytokines
Influence differentiation of blood
stem cells
IFN- and IFN-
Response to viral infection;
interfere with protein synthesis
IFN-g
Stimulates macrophage activity
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Immunological Memory
 Antibody titer is the amount of Ab in serum
 Primary response occurs after initial contact
with Ag
 Secondary (memory or anamnestic)
response occurs after second exposure
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Immune Responses to an Antigen
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Figure 17.16
Types of Adaptive Immunity
 Naturally acquired active immunity
 Resulting from infection
 Naturally acquired passive immunity
 Transplacental or via colostrum
 Artificially acquired active immunity
 Injection of Ag (vaccination)
 Artificially acquired passive immunity
 Injection of Ab
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Terminology of Adaptive Immunity
 Serology: The study of reactions between
antibodies and antigens
 Antiserum: The generic term for serum because it
contains Ab
 Globulins: Serum proteins
 Immunoglobulins: Antibodies
 Gamma (g) globulin: Serum fraction containing Ab
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